Abstract

Background

High altitude pulmonary edema (HAPE) affects individuals and is characterized by alveolar
flooding with protein-rich edema as a consequence of blood-gas barrier disruption.
In this study, we hypothesized that aquaporin 5 (AQP5) which is one kind of water
channels may play a role in preservation of alveolar epithelial barrier integrity
in high altitude pulmonary edema (HAPE).

Methods

Therefore, we established a model in Wildtype mice and AQP5 −/− mice were assingned
to normoxic rest (NR), hypoxic rest (HR) and hypoxic exercise (HE) group. Mice were
produced by training to walk at treadmill for exercising and chamber pressure was
reduced to simulate climbing an altitude of 5000 m for 48 hours. Studies using BAL
in HAPE mice to demonstrated that edema is caused leakage of albumin proteins and
red cells across the alveolarcapillary barrier in the absence of any evidence of inflammation.

Results

In this study, the Lung wet/dry weight ratio and broncholalveolar lavage protein concentrations
were slightly increased in HE AQP5 −/− mice compared to wildtype mice. And histologic
evidence of hemorrhagic pulmonary edema was distinctly shown in HE group. The lung
Evan’s blue permeability of HE group was showed slightly increased compare to the
wildtype groups, and HR group was showed a medium situation from normal to HAPE development
compared with NR and HE group.

Conclusions

Deletion of AQP5 slightly increased lung edema and lung injury compared to wildtype
mice during HAPE development, which suggested that the AQP5 plays an important role
in HAPE formation induced by high altitude simulation.